Basic components of storytelling.
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Above and beyond ST is a communication tool among human beings with a core aspect which is the emotions. “Serious” ST is an earnest narrative, a way to tell stories outside the context of entertainment. ST has different components such as narrative, perspective, interactivity, and medium. Narrative is the actual content of the story, which includes times-contexts, causes-effects, sequence, etc. Perspective refers to the fact that in each story the author conveys a subjective point of view of a certain aspect of the story. Perspective includes facets such as cognition, emotions, encoding-decoding, meaning, memory, etc. Interactivity is essential in ST, including story features such as engagement, modification/decision of narrative flow, etc. Finally, medium includes mediation, channels, forms, etc. When ST is defined as a narrative, two components must be considered: the narrative content (story) and the narrative form (discourse). Stories and discourses build a fundamental way for humans to make sense of the world (Table 1) [2].
Elements | Meaning | Instruments |
---|---|---|
Narrative | Content (story) Form (discourse) | Time-context Cause-effect Sequence |
Perspective | Subjective point of view | Cognition Emotion Encoding-decoding Meaning Memory |
Interactivity | Story features | Engagement Modification Narrative flow |
Medium | Means of communication | Mediation Channels Forms |
Basic components of storytelling.
Serious ST refers to a non-entertainment context, where stories are part of the real world. It aims to create mental models about different areas in which narrative elements such as engagement, conflict, characters, emotionality, meaning, cause-effect relations, and time and space constraints are adapted to convey experiences [1]. A narrative is a vehicle to trigger emotional and cognitive responses to achieve certain serious goals within their context of solicitation. In addition, interaction becomes a matter for decision processes, knowledge creation, communication of nonquantifiable facts, and altering narrative flow to achieve serious contextual goals. Context, course, content, and channel are the four essential components of serious ST. The context is basically the application of circumstances (e.g., medical or psychological problems); the course would be how content evolves in a cause-effect relationship as part of the application context; the content is the actual ideas contained in the narrative; and the channel is the kind of way to communicate stories [1, 2].
With respect to the context, the applications of serious ST in well-being, health, medicine, and psychology are good examples of the multiple possibilities in this field of study [3, 4]. From a scientific point of view, and following Dahlstrom et al., we prefer using the concept of “scientific storytelling” when we apply it in medical investigation [5].
The objectives of our reflection were to propose ST as a tool to offer family support in eating disorders (ED) and to describe the development of the story-based interventions targeted to families (developing communication strategies). It must be noted that ST is a way to communicate (mainly emotional narratives) but not a specific therapy for ED.
With respect to the method, due to the fact that this chapter is based on a future review, which we are developing (“storytelling and health education”), the main data of our reflection are taken from a search using PubMed/MEDLINE and PsycInfo, considering those articles mainly focused on ED and specifically on bulimia nervosa.
The effectiveness of ST as a communication tool in healthcare has been supported by evidence from several disciplines [6].
Within the healthcare context, ST might be seen as a way of assistance in learning about and managing one’s disease or a relative’s disease. ST aimed to disease management is based on the fact that each person has his or her own unique experiences living with and managing a disease; the same applies for relatives. Thus, patients and patient relatives’ stories are a relevant information source to both patients and families [7].
In this way, storytellers are patients and patients’ relatives who suffer together a disease or disorder. By identifying with the storyteller, participants can become invested in the content and be positively influenced by the self-management actions described. Telling stories, emotional stories, is a very good tool to break down cognitive resistance to messages promoting lifestyle and behavioral changes [7] or, many times, to get involved in adequate care and support. Through ST, patients increase their receptivity to the health information contained in the stories as it occurs among patients’ families.
In sum, ST is a way to motivate both patients and families [6]. In this regard, ST, as a mechanism for reduction in change resistance, is related to health outcomes [7]; it makes patients and families more inclined to follow strategies that have worked for others (and perhaps they have previously avoided) [8]; it reports mutual benefit (discovery and exploration of new information, practical management strategies and skills, opportunities for adoption of resolutions, etc.) when patients/families exchange their health-related stories [9, 10, 11].
When ST is developed in a group format, several authors have reported different benefits [12, 13, 14, 15]:
ST might establish a network of trust and equality among participants, and it would be a way of cohesion among participants.
ST tends to reduce stigma associated with diseases, and it facilitates the development of relationships among the participants.
ST can naturally facilitate peer support and enable a support network to form.
The peer support obtained by means of ST might encourage participants to examine their emotions, problem-solving skills, and goal setting and exchange social support, all of which are core self-management components within health-related contexts.
In summary, ST focuses on the patient’s perception of their unique needs and their ability to self-manage their disease and similarly occurs when ST is applied to patients’ families. Consequently, ST facilitates both patients and families to develop strategies to manage their illness and suffering, respectively [16].
Chronic diseases usually require regular contact between patients/families and therapists. In this particular way, ST could be a good approach for both patient self-management and family management. For this proposal, core principles of ST, when applied to health contexts, have been reported to be social cognitive and ecological theories of health behavior, caring and healing, and narrative-autobiographical approaches [17, 18, 19, 20]. There are two main objectives of ST in health interventions: (a) to get patients/families to reflect the illness experience and (b) to create meaning from it [20].
As Gucciardi et al. have reviewed, health conditions such as diabetes mellitus, cancer, multiple sclerosis, or psychiatric disorders are frequent diseases in which ST has been applied [20]. Sessions of ST are based on informal-spontaneous sharing of stories by means of a nondirective facilitation approach. Sessions do not consist of didactic delivery of information even though “facilitators” (doctor, nurse, dietitian, etc.) can respond to the shared stories and they can also provide information if required. In this context facilitators play a role of equality but not of experts. Finally, ST must have some elemental rules such as trust, respect, empathy, and no judgment [12, 20, 21]. Sometimes it is possible to use “peer facilitators” (e.g., patients’ relatives) previously trained as health promoters and, of course, in ST [12].
Sessions of ST applied to chronic diseases tend to be given over 5–15 weeks, with each session lasting 1–2 hours. The environment usually is an open atmosphere, thus giving everyone the opportunity to speak about their experiences. It is convenient to select topics in advance in order that participants prepare the session with the story (or stories) they want to share in the group (e.g., diagnosis experience, course of the disease, family stress linked to the therapeutic aspects, etc.) [22]. The way to share stories is diverse: verbally, by means of action-oriented activities (e.g., cooking, exercising, etc.), using pictures, writing, trough songs, poems, and readings. ST is not a mere colloquium; it is a participant-centered technique of communication where patients and families are encouraged to self-reflect on their personal experiences.
In the context of chronic diseases, ST is not a way of simple catharsis. Telling stories about illness experiences seems to be therapeutic due to its potential to facilitate learning and coping with the disease. As it was noted by Gucciardi et al., ST is a process of unearthing meaning in the lived experience of illness [20]. Telling stories triggers the reflection and understanding of oneself and the disease [23]. The process of ST starts as a single story (my story), and then stories are elaborated by group participants thus becoming a shared experience [21]. Different ages, groups, ethnicities, socioeconomic status, or gender are potential participants of ST applied to health problems. With respect to ideal number of sessions, basing on participants’ preferences and bearing in mind the complexity of the self-management of the disease are better. As it was abovementioned, the use of verbal and written formats is the main strategy along with pictures or photographs [20].
The role of narratives has grown in relevance since the 1980s due to the importance of illness experiences. It must be noted that narratives reflect the nature of the chronic disease experiences but also can be a part of it [24].
Traditionally, families are considered to play a key role in the management and treatment of ED. Families do not suffer from an ED, but they live with an ED. In this regard families’ stories are a way to create experiences, experiences linked to the emotions which usually accompany a life with an ED.
In the field of ED, families have been associated with relationship alteration within the family, problems between partners, great stress experience, problems to cope successfully, uncertainty regarding recovery progress, parental blaming, etc. [25, 26, 27, 28, 29, 30]. ED, as it occurs generally in chronic diseases, might be described as a form of biographical disruption which breaks individual or family-anticipated life paths. As a consequence, narratives lose coherence and meaning and identity becomes lost. The result is a new narrative incoherence which will imply a narrative reconstruction. Stories, ST, will provide new coherences thus giving meaning to ED [31, 32].
Frank [33] considered three narrative types with respect to stories of illness: restitution, chaos, and quest. The first seems to be dominant, and, in sum, it consists of sentences such as “yesterday I was healthy, today I am sick, tomorrow I will be healthy again.” On the contrary, chaos narrative is the opposite of restitution, something like “life never will go better again.” In this case there is not a narrative coherence to explain the illness. Finally, the quest narrative implies that patients see illness as an opportunity to believe that something is to be gained from the illness experience. Telling stories such as restitution, chaos, or quest narratives has not the same results. Each one shapes experiences. Thus, restitution narratives are usually associated with the fact to pursue, be hopeful, and expect recovery. If the narrative of storytellers shapes their own experiences, the same occurs with regard to the listeners, who, in turn, would also modify their illness experiences [33, 34].
It has been established that ED affect all facets of life and they are a challenging experience for the whole family [34]. It is frequent that parental understandings of illness can remain couched in restitution. Nevertheless, when family members construct ED differently to each other, the consequence is the conflicting narratives and, finally, frustration, anger, and altered communication [34]. Considering the three narratives as suggested by Frank [33], it is possible to observe a process during the therapeutic work in ED (Figure 1).
Therapist working with ED. Adapted from Papathomas et al. [34].
ED are usually chronic disorders, thus being both a challenge and a source of family problems. Within the family system, a process of meaning-making will emerge which is absolutely necessary to cope with the illness. This process is guided by culturally dominant illness narratives as stated by Frank [33].
When patients with ED are the storytellers, it is possible to distinguish two very different narratives: the discourse of anorectic and bulimic patients [35, 36].
The discourse of patients with anorexia nervosa is built upon three pillars: intensification, circularity, and polarization. This discourse presents a defined reality characterized by excess, conflict, and closing [35].
Intensification leads to derealization, thus showing a distorted world with regard to its dimensions. On the one hand, it is a vehicle to express very intense feelings; on the other hand, intensification does not end up with this expressive function since it serves as a strategy to legitimate specific behaviors [35].
The amplified image of reality triggers the alarm; it expresses an obsessive fear to gain weight. Thus, body image is perceived to the limit of bearable, and this seems to justify the obsessive desire to lose weight. Maybe the discourse shows the object: the distorted image acts generating fear, thus becoming a relevant factor which maintains the disorder. The dichotomic vision of reality reinforces anorectic behaviors since that vision implies a fight between contrary parts. The result is an experience of a fragmentary world and a split-off vision with respect to the own conscience. Antithesis, paradoxes, and generally the dialectical approach keep alive and reinforce the awareness of both external and internal confrontation, and, as we have seen, once the conscience is divided between opposing parts, it is always defeated in this war of no one [35, 36].
Circularity, showed linguistically by a high degree of recurrence, creates a net of words which envelops and imprisons. As the water of a fountain reflects the image of Narcissus, anorectic discourse throws an image which locks one inside; that discourse shows a conscience turned on itself, tightly centered and closed on the conflict. From this point of view, anorectic discourse is both an expression and an instrument of the disease. At the same time, that discourse has the keys which might neutralize the disease effects. If the discourse catches and it makes the person sick, it is possible to build another different discourse to create and legitimate a healthy behavior.
Considering positive and negative elements of anorectic discourses, it would be possible to include the analysis of discourse within the whole treatment program. By means of the analysis of recordings and texts, it is possible to think over with a critical point of view about the patients’ thinking schemes. Then it would be possible to build an alternative discourse, a new healthy discourse [35].
In the case of bulimia nervosa, as a feature that defines the discourse, its openness from the thematic point of view and also some peculiarities in what refers to the global construction of the discourse should be noted. From the thematic point of view, stories usually show a universe open to others, with a central theme, which is dependent on affection and recognition of others [36].
Following the studies of Márquez [35, 36], considering bulimia nervosa, perhaps the most outstanding feature, along with the fragmentary character of the discourse, is the polyphony: voices of the same person or of the others, real or imagined, that give life to the story, make it rich and complex, and, at all events, show a consciousness inhabited by others, confused with them.
In the syntactic plane, the global organization of the discourse is defined by its scattered character: broken syntax with unfinished structures, suspended utterances, and sudden alterations in rhythm show a specific type of thought which is built on impulses.
Verbalization of experiences, reflection, and reconstruction of memories are emerging to consciousness in a choppy way, in various attempts that are not usually alternatives to saying the same thing (or different ways of approaching a fact), since the first tend to be unsuccessful. Stories are characterized by impulsivity, ruptures, advances, and setbacks, which, in short, express precipitation, lack of a necessary prior time for reflection and planning, lack of containment, and difficulties in adjusting to limits.
Intensification presents facts and sensations as endowed with an extreme force; as a result, reality is constructed with such intensity that it is uncontainable within its natural channels. Thus considered, this resource serves as legitimization of the illness behaviors. Vocalic lengthening and sudden changes in the language rhythm, as well as precipitation and slowing down, also show the presence of emotions that overflow the consciousness, sensations, and affects that are difficult to conduct and finally become not contained.
In short, a broken speech seems to reflect the lack of a coherent internal organizing center, a broken voice, a word that has its justification and its center abroad, as an echo [36].
From a dialogical view of change, it is possible to consider change and resistance to change. Resistance to change derives from the slavery of repeating, which traps the dialogical self. The tension between change (liberty of reborn) and resistance to change (self-determination to repetition) can be also represented as voices discussing and contrasting in the context of a personal arena, in the dynamic of a dialog between parts [37].
It is usual to work with families when an ED patient begins his/her process of treatment. There are two facts which we can observe at this point. Firstly, families tend to express that they never imagined a son or daughter with an ED. Second, it is frequent that families talk about their “fault.” Novelty and fault build a recurrent question: Why?
It has been said that healthy relationships are like the tides: they ebb and flow, especially when it comes to verbal interaction. Ebbing and flowing give as a result a balance. But when a family member suffers from an ED, this balance is very hard to maintain. When this occurs, the patient becomes quite self-centered, self-absorbed. Now, relationships as well as dialogs need to be rebalanced. Once an ED affects a family member, many times siblings are victims of that ED since parents focus much more of their time, thoughts, and energy on that affected member. Verbal interactions and relationships are strongly modified. From the point of view of siblings, the patient gets all the love, all the attention, while other members get ignored and overlooked. In order to attract parents’ attention, siblings may start some unhealthy behaviors such as rebelling, acting out, etc. [38].
ED often is an enemy of healthy relationships. As an ED develops and progresses, it often takes the place of wholesome relationships that may have once existed in one’s life. Typically, as the ED roots within a person, relationships with family members, friends, partners, etc. become strained and gradually altered [39].
Altered relationships within the family tend to create a different discourse. The coherent healthy discourse becomes a broken discourse stained by feelings of doubt, guiltiness, and many times lack of hope. This way a new story emerges. Patients, siblings, parents, partners, etc. have their new particular stories to tell or, sometimes, shut up. During the therapeutic process of ED, there are very different elements that parents refer to as having a great impact on their lives. Examples of these elements would be family unification or disintegration, inability to cope with the disease, inconsiderate comments from significant others, social isolation, and financial impacts, among others. The chronicity of ED causes stress for the family as a unit, by affecting the family’s coping mechanisms and the family’s relationships with significant others leading to isolation of the family unit [28].
Isolated parents give few insights into the ED experience across the whole family unit. Illness experiences may be analyzed through thematic analyses. Although these content-driven approaches can be useful, they offer scarce for the social construction of the ED experience. Specifically, how personal interpretations of illness are shaped through social and cultural narrative auspices is rarely addressed. It is in this regard how ST would be an appropriate tool to understanding illness. The role of narratives, the role of telling stories, would lead to the deepest personal illness experiences. Narrative therapy for ED is well known since the 1980s. By means of telling stories, therapists work with patients, who create a sort of “anti-anorexia” and “anti-bulimia” stories. These stories aim to depict a separation between the person and the disorder, thus setting up space for patients (and families) to re-envision their relationship with their ED. Patients will create a new personal story “without the ED.”
Along with bulimia nervosa, it has been reported that 61.5% of youth with this ED could be considered to have one or more comorbid disorders (especially mood disorders, anxiety disorders, and personality disorders) [40]. In this particular way, ST might be applied not only in the case of bulimia nervosa but also when comorbidities are present. Thus, using narrative therapy in a group of women with long-course ED with comorbid depression, a reduction in both ED and levels of depression was obtained. It seems necessary to work with different facets: (a) externalize the ED, thus creating distance between herself (patient) and the disorder; (b) explore the person’s ED, in which values belong to the patient and which belong to the ED; and (c) develop an alternative story to support the client’s sense of self (not just with respect to eating but in other areas of her life); it is not the same “to be” a bulimic patient than “to suffer from bulimia nervosa” [41].
ST is a way of communication, a way to change the discourse, thus contributing to change our mind. Many patients usually say “I can’t start again” and “it is impossible to change.” But if the patient does not change, the result is the permanence. The same applies to families. Between change and permanence emerges the conflict, and the discourses serve the conflict becoming broken, incoherent. Stories may be based on change and on no change. The consequent discourse is a speech aimed to express the deep desire of change or, on the contrary, the conviction to permanence, the change being impossible. As Marquez stated [35, 36], change vs. non-change is something like an inner dialog between voices, but not only “inner” since external components appear (family, partner, friends, etc.). As stated by Salvini et al. [37], the dialog between voices implies that when one party speaks, the other party is required to be silent. This way, it is common that a dominant discourse emerges (interactional dominance), the dialog being asymmetrical. Therapists must consider this phenomenon because the more symmetrical the dialog is, the more opportunity it provides for mutual influence; the more asymmetrical it is, the more it constrains the exchange of views and experiences. When symptoms are the core part of the discourse and this discourse becomes dominant, patients and families are imprisoned. Following the analysis of Márquez [36], in bulimia nervosa stories are characterized by impulsivity, ruptures, advances, and setbacks, which, in short, express precipitation, lack of a necessary prior time for reflection and planning, lack of containment, and difficulties in adjusting to limits. This style usually leads to a chaos narrative [33].
Based on the study of Hermans et al. [42], Salvini et al. [37] considered the trend toward discursive change during the therapeutic process according to the following four dimensions: (a) interactional dominance, (b) topic dominance, (c) amount of talk, and (d) strategic movements. In a process of scientific ST, it is relevant to analyze linguistic variations probably linked to a transition from a dysfunctional narrative to a new more coherent one. Among a group of bulimic patients (here bulimic storytellers), one of them could be dominant, and the dialog starts being very asymmetrical. With respect to the topics, diets, body image, emotional instability, binge episodes, purging, and other altered behaviors (e.g., self-injuries) are usually highlighted by group members. At the beginning the amount of talk and strategic movements might be summarized as a scarce of true dialog with different attempts to impose one over others. Each member seems to search for a top position in the group, thus polarizing and dominating the other voices [37]. As the sessions go on, a more reciprocal interaction is favored. The topics remain but they are less strong than before. In order to understand these changes, it is necessary to bring here the concept of metaposition, something like a “third voice.” This third voice has a reflexive function. Some auxiliary verbs (I have to be treated, I want to get better, etc.) are contrasted by more verbs which imply personal conditions (I feel happy, I do not like, etc.). With the progression of the ST process, the preferred tense is the past, thus distinguishing between a previous condition and the current state (when I binged, once I felt frustrated and I used laxatives, etc.). Step by step a passage from a condition of dysfunctional self-narratives to more organized ones is observed.
As reported by Marquez [36], the discourse may have a relevant role in maintaining the problem, but it is possible to pass from a broken discourse to another healthier one. The discourse reveals psychological profiles as well as interaction styles. In the field of ED, and particularly in bulimia nervosa, working with ST should aim to introduce a “language of change” for both patients and families.
Characteristics of bulimia nervosa involve the sufferer bingeing on large amounts of food, during which patients experience feelings of extreme loss of control. Bingeing leaves the patients feeling guilty, disgusted with themselves, and afraid of weight gain. Patients try to compensate for this by vomiting, by exercising, by fasting, by abusing laxatives, or often by some combination of these behaviors. The life of bulimic patients is usually chaotic: dieting, bingeing, purging, fear to weight gain, feeling of being fat, etc. As result, patients have a negative view of themselves which usually leads to avoiding social interactions. Low mood and poor quality of life complete this framework.
In a ST group, some topics will emerge soon:
What is bulimia nervosa?
Effects of bulimia nervosa in my life (physical, psychological, and social facets)
Dieting
Is it possible to change my way of thinking?
What are thinking errors?
Coping with problems and emotions (anxiety, depression, fear, etc.)
Body dissatisfaction
Assertiveness
How is my future?
Can I help myself?
Bulimia nervosa has many disadvantages for me but has it any advantages?
What is a vicious cycle (diet-binge-diet; purge-binge-purge, etc.)?
What induces me to binge?
What triggers diet-binge-purge?
Can I remember what is normal eating?
Is this a healthy life?
Am I aware of the links among feelings, thoughts, mood, behavior, relationships, etc.?
In ST “emotional meanings” are essential. Patients with ED assign different meanings to their disorder. Those meanings are reflected in their narratives, their illness experiences told in their particular stories. Patients with bulimia nervosa usually have maladaptive thoughts and emotions related to eating habits and body weight. They also have low self-esteem, and they seem to be sure that a well-designed body would be a remedy for their problems of personal insecurity. In this regard, their behaviors aim an idealized body through diets, purging rituals, and often strenuous exercise. The chaos is based on the fact that the desire to lose weight is associated with a personal disorganization. As a result, regulation and control over eating become an attempt to organize and stabilize the chaotic mental state [43]. ST is a good instrument to communicate emotional experiences and a way to access patient’s difficulties and internal conflicts. In fact, narratives can be seen as expressions of the self and the living experience for the individual who narrates. The link between individuals and their “bulimic (or anorectic) voice” could explain their ambivalence to change [44, 45, 46].
Apart from the abovementioned topics related to the patient’s current problems and family-related features, there are different meanings with respect to the onset of the disorder. Low self-esteem, clusters of stressful events, new experiences/difficulties emerged with the disorder, feelings experienced after the onset of the disorder, etc. are usually core parts of the patients’ narratives [43].
As other therapeutical approaches, ST aims to produce changes. Patients and families could expect changes to happen such as more dialog, closeness and affection between family members, fewer conflicts between siblings, greater family participation in treatment, more family togetherness, less critical comments, etc. Considering families, the desire to change family dynamics seems to facilitate a healthier environment and consequently a clear improvement in the therapeutic progress. Generally, family emerges as the main source of patients’ social support.
ST is a communication tool among human beings with a core aspect which is the emotions. Narratives are a vehicle to trigger emotional and cognitive responses to achieve certain serious goals within their context of solicitation. With respect to the context, the applications of scientific ST in well-being, health, medicine, and psychology are good examples of the multiple possibilities in this field of study. Considering health contexts, storytellers are patients and patients’ relatives who suffer together a disease or disorder. In this particular way, ST is a manner to motivate both patients and families, ST being a mechanism for reduction in change resistance, which is usually related to health outcomes. In the context of chronic diseases, ST is not a way of simple catharsis. Telling stories about illness experiences seems to be therapeutic due to its potential to facilitate learning and coping with the disease. ED are usually chronic disorders, thus being both a challenge and a source of family problems. Within the family system, a process of meaning-making will emerge which is absolutely necessary to cope with the illness. This process is guided by culturally dominant illness narratives as stated by Frank, and it was abovementioned [33]. As reported by Marquez [36], the discourse may have a relevant role in maintaining the problem, but it is possible to pass from a broken discourse to another healthier one. The discourse reveals psychological profiles as well as interaction styles. In the field of ED, and particularly in bulimia nervosa, working with ST should aim to introduce a “language of change” for both patients and families. As it was abovementioned, impulsivity, ruptures, advances, and setbacks, which, in short, express precipitation, lack of a necessary prior time for reflection and planning, lack of containment, and difficulties in adjusting to limits, are a cluster which define the interaction between family members and a patient diagnosed with BN. This style usually leads to a chaos in both narrative and relationships (in the case of anorexia nervosa, the circularity—manifested linguistically in the high degree of recurrence—weaves with words a network that envelops and imprisons; the discourse projects an image that encloses the subject within himself; the discourse shows an awareness turned inward, hermetically centered and closed on the conflict, thus affecting a clear dialog with others) [35, 36]. In sum, ST aims to produce changes, in both discourse and relationships. Patients and families could expect changes to happen such as more dialog, closeness and affection between family members, fewer conflicts between siblings, greater family participation in treatment, more family togetherness, less critical comments, etc. Considering families, the desire to change family dynamics seems to facilitate a healthier environment and consequently a clear improvement in the therapeutic progress. Generally, family emerges as the main source of patients’ social support.
ST is above and beyond a useful form of communication. ST is not a specific therapy, and its great advantage is to improve the existing therapies by means of a better communication between therapists and patients as well as between family members and patients. With respect to ED, a patient (that is to say a “storyteller”) could summarize, in a delightful poem, the process of changing of someone who starts suffering from anorexia or bulimia nervosa (and still is sure to control it) until they reach a point of no return. The capital letter of each verse wants to reflect the inner highness of the affected person.
Due to the original language in which the poem has been written down, we have decided to maintain the Spanish version as well as to translate the poem into English.
I WISHED TO BE…
And I wanted to be waning moon just not to be sun.
And I imagined myself to be fine and delicate rainfall.
And I was a beautiful Caladium with a slender stem.
And I dreamt of being a horse chestnut tree with an upright and leafy trunk.
And I tried to be Artemisa or Apollo.
But I became a goldfinch that could not sing and my colors faded without my knowing why.
And ceased being an Alpha Canis Majoris when my shine dimmed.
When the failed transformation occurred.
All the figures that my mind reflected were slimline.
Until I did not want to be, until I did not think.
Because I was just looking for perfection.
Y QUISE SER…
Y quise ser luna menguante para no ser sol.
Y me imaginé ser lluvia fina y delicada.
Y fui hermosa Caladium de tallo esbelto.
Y soñé ser un castaño de Indias con el tronco erguido y abundante hojas.
Y fingí ser Artemisa o Apolo.
Pero me convertí en un jilguero que no podía cantar y perdí mis colores sin saber la razón.
Y dejé de ser una Alpha Canis Majoris cuando perdí mi brillo.
Cuando sucedió la transformación fallida.
Todas las figuras que mi mente reflejaba eran finas.
Hasta que no quise ser, hasta que no pensé.
Porque solo buscaba la perfección.
The journey of exploring acid and base starts long before, but in the last century the advancement was remarkable. In 1890, Wilhelm Ostwald electronically measured hydrogen [1]. Svante Arrhenius won the Noble prize in 1903 for the theory of ionization [2]. In 1908, Henderson and Black showed that bicarbonate and phosphate equilibrated with CO2 at normal body temperature in different solution [3]. In 1923, Bronsted first put forward the idea of acid as a substance that ionizes in solution and donate hydrogen and the base accepts the hydrogen from the solution [4]. Bronsted, Henderson and Van Slyke described acid-base balance in the early part of nineteenth century [5]. Handerson invented bicarbonate as the most important buffer system of the body, and Hasselbalch first measured the real blood pH in the early part of nineteenth century [6, 7, 8]. In 1909, S. P. S. Sorensen developed the pH scale [8]. Later Hasselbalch-Henderson developed an equation that helped in relating pH to the blood bicarbonate and PCO2 [7, 9, 10]. In the early 1980s, scientists introduced electrodes specific for each ion. Thereafter, serum electrolyte and the anion gap measurement become routine tools for assessing acidosis.
Acidosis has fatal consequences like CNS damage. Even death is not uncommon. Acidosis is characterized by a decrease in pH, and this change is rapidly corrected by the body buffer systems. Many clinical conditions develop acidosis, as well as ionic derangements and the only correction of the underlying cause can resolve it. There are equal numbers of cations and anions in the blood and among them there are some unmeasured anions. These unmeasured anions can contribute in the clinically important anion gap. In a healthy individual, there is an acceptable range of normal anion gap. But some conditions can increase or decrease this gap. Increased anion gap usually represents metabolic acidosis. Albumin and many other confounding factors influence the anion gap derangements. Accuracy in measuring anion gap is critically important for the evaluation of acidosis.
The body maintains its normal physiology by the strict balance of acid and base. The body maintains its normal arterial pH close to 7.4 at a range between 7.36–7.44, and the intracellular pH of the human body is 7.2 [11]. Normal acid-base balance is the balance between each hydrogen increase by the intake or production, and that is decreased by elimination. Acid-base balance is measured by measuring pH, CO2 and HCO3. In general, consuming animal protein add acid in the body, and consuming cereals and vegetables add alkali in the body. In oxidative metabolism, CO2 is produced in the tissue, and at a similar rate, that is eliminated by the lungs. So, pCO2 persists at about 5.33 kPa (40 mm of Hg). Different buffer systems of the body play a crucial role in removing excess H+. Metabolism of carbohydrate and fat uses O2 and produce CO2 and H2O. Normal lungs efficiently remove most of the CO2. In oxidation of amino acids, carbon dioxide and water are produced along with the liberation of nitrogen as ammonia, a toxic material in the body. In the liver, the urea cycle utilizes the ammonia, where this toxic NH3 combines with CO2, and produce urea. In the proximal tubule and other renal epithelial cells, ammonia and bicarbonate are also produced from glutamine metabolism. Some of it returns to the body fluid through the renal veins and is metabolized in the liver. And the rest of the NH3 excreted in the lumen. So, NH3 does not exist in the body fluid. Most of the NH3 is excreted in the urine, and it plays an important role in removing H+ to maintain normal acid-base balance. In the urine, NH3 binds hydrogen ion to produce NH4, and it prevents excessive acidification of urine.
Excess acid is eliminated from the body by the lungs and the kidneys. In the lungs, acid is eliminated in the form of CO2, and in the kidneys, acid is excreted as acid phosphatase and ammonium. CO2 is lipid soluble, and it crosses the cell membranes in the lungs. Most of the CO2 produced in the tissue is eliminated by alveolar ventilation. Arterial and brain chemoreceptors can sense the acid and base excess, and respiratory system responds with hyper or hypo ventilation. As a result, pH is increased or decreased by increasing and decreasing pCO2 level. The regulation between CO2 and H2CO3 level is critically maintained when the blood travels through the lung capillaries. When strong acid is added, some HCO3− become H2CO3 and blood PCO2 is increased. In acidosis, carbonic acid dissociate to CO2 and H2O. As a result, respiratory center is stimulated and it leads to hyperventilation. Hyperventilation eliminates these CO2 to maintain normal pH. In alkalosis, CO2 is retained by hypoventilation. This CO2 combines with H2O to produce H2CO3, and pH is maintained.
The kidneys excrete acids, both respiratory and nonrespiratory origin and retain HCO3− to stabilize the pH of blood. HCO3− is predominantly regulated in the kidneys. The nephron reabsorbs all filtered bicarbonate in exchange for H+. The kidneys also produce new bicarbonate to neutralize acids. Tubular cells contain carbonic anhydrase, that converts CO2 and H2O to HCO3− and H+. Newly formed HCO3− is shunted to peritubular capillaries and H+ is excreted in tubular lumen. Bicarbonate is also produced from glutamine metabolism along with ammonium. Some NH4 diffuses to body fluid and converts to urea in the liver. The rest of the them excreted in urine. The tubules are impermeable to bicarbonate, and it cannot be converted back to CO2 and H2O. So, the blood HCO3 level is increased.
In the apical membrane of the kidney tubules, sodium is reabsorbed in exchange for the hydrogen ion. Salts like sulfates, phosphates, ammonia combines the hydrogen ions and excrete it. The kidneys titrate less than half of the excreted acids and the rest is excreted as ammonium [11]. For every ammonium excreted in urine, one HCO3+− is reabsorbed. HCl and H2SO4 are produced during dietary protein metabolism reacts with NaHSO4, and produce NaCl and Na2SO4. These Na salts are excreted by the kidneys as NH4Cl, and (NH4)2SO4.
The kidneys are largely responsible for K+ excretion and most of it is reabsorbed in the proximal tubule and in the loop of Henly. In acidosis, K+ secretion is decreased and K+ absorption is increased in the collecting duct. In alkalosis, hypokalemia develops from increased K+ secretion and reduced K+ absorption in the collecting duct. H+ and K+ exchange occur in the tubules. Serum potassium level also influences the renal acid-base balance. In hyperkalemia, potassium is available in an increased amount in the filtrate, and hydrogen will be scarce for exchange with HCO3 and there will be an imbalance. In hypokalemia, less potassium will be available for H+ and K+ exchange and hydrogen will be available to exchange with bicarbonate.
Na+, K+ and NH4+ are the principle urinary cations, and the principal urinary anion is chloride. Urinary anion gap helps in estimating renal NH4+ excretion, as NH4+ is the urinary unmeasured ion. Chloride is an important anion in neutralizing positive ions, reabsorbed in the proximal convoluted tubule and secreted in urine by the collecting duct. Secreted H+ is also buffered by urinary buffer HPO4− to H2PO4, and is excreted in urine.
Acidosis results from a reduction in serum bicarbonate and cause secondary reduction of PaCO2 resulting in a low blood pH. It develops from the addition of hydrogen or removal of HCO3 from the body. PaCO2 in blood is 38 ± 2 mm of Hg and HCO3 is 24 ± 2 mmol/L. Metabolic acidosis is characterized by the blood pH <7.38 and bicarbonate <22 mmol/L [12].
Acid and base disorders are: respiratory acidosis and respiratory alkalosis, and metabolic acidosis and metabolic alkalosis [13]. In respiratory acidosis, PaCO2 is increased and it is compensated by renal H+ excretion, HCO3 retention and HCO3 generation. In respiratory alkalosis, decreased PaCO2 is compensated by renal HCO3 excretion. In metabolic acidosis, HCO3 is reduced and it is compensated by hyperventilation and PaCO2 reduction. HCO3 is increased in metabolic alkalosis, and it is compensated by increasing PaCO2 by hypoventilation [14]. Usually, respiratory disorders cause derangements of CO2 level in the blood, and change in HCO3 level is developed from metabolic disturbances.
In the blood, Alkali is present mainly in the form of sodium bicarbonate, and bicarbonate is bound to other bases. Increase in BHCO3 and decrease in H2CO3results in alkalosis, and decrease in BHCO3 and increase in H2CO3 results in acidosis [13]. The body contains many acids. They are hydrochloric acid, carbonic acid, citric acid, lactic acid, phosphoric acid and carboxylic acid. Acute metabolic acidosis is developed by the overproduction of organic acids, like lactic acid and keto acid. Chronic acidosis is caused by bicarbonate wasting and impaired urinary acidification.
Blood cells are more acidic than serum, which influences the distribution of electrolyte and water between them. These transports took place with the oxygenation and reduction of hemoglobin and shift of bases (Na+, K+) due to changes in pH. Under normal environment Na+ and K+ do not diffuse through the cell wall. Shifting of water and electrolyte through membrane results from the change in anion (HCO3− and Cl−) and H+ concentration, and that changes in cell volume. CO2, relative electrolyte concentration and weak acid concentrations are three independent variables that regulate blood pH [15].
The body has different buffer systems to maintain the normal pH of the body. Elkinton Jr. reported that multiple level of buffering linked different series of ionic exchanges which includes hydrogen, sodium, potassium, and other anions. The buffers absorb excess hydrogen and hydroxyl ions. They help in the maintenance of neutrality during redistribution of the hydrogen ion [16].
A buffer system consists of a weak acid with its conjugate base, or a weak base with its conjugate acid. Blood is a strong solution, and it has many important components that maintain the buffer systems. These include hemoglobin, bicarbonate, carbonic acid, plasma proteins, RBCs and plasma phosphate [17]. HCO3/CO2 buffer is the most important buffer system of the body, and plays a major role in regulating pH of the blood. But, the rest of the buffer systems have minimum contribution in pH regulation. In dissolved state, bicarbonate and carbon dioxide ion remains in equilibrium. Bicarbonate reduces strong acid to carbonic acid, whereas carbonic acid neutralizes strong base (Eq. (1)).
When CO2 and water is converted to HCO3 and hydrogen ions, this hydrogen ion is then buffered by hemoglobin [18].
Proteins have a buffering capacity, including hemoglobin. Protein can accept and donate H+, if there is H+ excess or it is reduced. Hemoglobin has a distinct types of buffer action. When blood passes through the capillaries, it loses oxygen and took CO2 to raise the PaCO2 and maintain the pH. Hemoglobin plays an important role in transporting both oxygen and carbon dioxide. In 1914, Douglas, Haldane and Christiansen tried to prove that the hemoglobin binds more CO2 in the reduced form than the oxygenated form [19].
The phosphate buffer system works in the internal environment of all cells. But, in the blood H2PO4− and HPO42− are found in a very low concentration. Sodium dihydrogen phosphate neutralizes strong bases and sodium monohydrogen phosphate neutralizes strong acids. The Phosphate buffer system plays an important role in the kidneys.
Two types of variables, dependent and independent, are important in acid-base balance [20]. Bicarbonate, hydroxyl ion, hydrogen ion or pH, weak acid, anion and carbon trioxide are dependent variables and they are determined by three independent variables pCO2, total weak acid and net strong ion charge [21]. Lungs, kidneys, liver and gut regulated this balance. Traditional bicarbonate/carbon-di-oxide approach, base excess approach and Stewert’s physicochemical methods are widely discussed for measuring the acid base disorders as well as to explore the physiology of body fluid.
HCO3/CO2 buffer system is the basis of this approach. Carbonic acid freely moves in the body fluid and dissociates into bicarbonate automatically when needed. Bicarbonate in the body acts as alkaline reserve. CO2, pH and HCO3 can be calculated by Hasselbalch-Henderson Equation (2) [7, 9].
This equation states that not only HCO3 and CO2, but also their ratio determines the pH. In this equation, PCO2 is the respiratory component and HCO3− is the metabolic component of the acid base imbalance. This buffer system is the largest and independent buffer system of the body and whole body acts as an open system for CO2. In traditional approach balance is determined by the influx and efflux of H+ and HCO3.
Astrup and Siggaard-Anderson introduced base excess approach, which is close to the traditional approach [22, 23]. Base excess can be calculated from bicarbonate concentration and pH of the body [4]. It can estimate the acid base status of non-respiratory origin. If base excess is too high, then it is metabolic alkalosis. If base excess is too low, then it is metabolic acidosis. When a deviation of normal blood pH is corrected by administrating base, then it is called base deficit. Which is a characteristic of metabolic acidosis. Base deficit with increase anion gap suggest the addition of acid in the body fluid. If there is a base deficit with normal anion gap, then there is bicarbonate loss from the body.
Here H+/proton is the preliminary determinant in acid base disturbances, not the CO2 [21]. The dependent variables are H+, OH−, CO32−, HA (weak acid), A−(weak anions), HCO3− and pH. The independent variables are strong ion difference (SID), total non-volatile weak acids (Atot) and PaCO2 [24]. Among them the strong ion difference has maximum effect on the hydrogen ion concentration. With that, acid base disorder can be divided into three categories: 1. respiratory (increase or decrease PaCO2), 2. SID changes (excess or deficit of strong ions or water) and 3. inorganic phosphate or albumin deficit or excess (Atot changes). In Stewart approach, a large number of variables are needed to calculate SID. Sodium, potassium, calcium and magnesium are strong positive ions, and chloride and lactate are the negative ions [25]. Bicarbonate and albumin are the balancing ion in strong ion difference. Strong ion difference (mEq/L) = [strong cations] − [strong anions]. Weak acid dissociates in body fluid (Eq. (3)).
A− Resembles weak anions, that vary with pH. Strong ion difference is filled with this weak A−, and HCO3+−, H+, OH−, CO32− are also present in minute amount, but are less important. There are many unmeasured anions accounts for ion difference. For electrical neutrality, strong ion difference and the total charge of weak ions must be equal [26]. Normal SID is dominated by sodium and chloride. But other negligible, but measurable ions are present there. Here narrowing of SID from an increase in [Na+] has alkalizing effect, whereas an increase in [Cl−] has acidifying effect. From the ionic basis metabolic acid base disturbances are about four major types [25]: (1) The water effect, and it is produced by dilutional effect on SID. Free water intake and intravenous infusion can produce it. (2) The chloride effect is caused by chloride change, and administration of normal saline is the common cause. (3) The protein effect is produced by a change in albumin concentration. (4) There are other factors, and those are influenced by unmeasured anions, that cause a wide anion gap.
In vivo, true ion gap cannot exist. There are many anions and cations in the blood. Blood cations and anions must be equal. Sodium, chloride and bicarbonate have the highest concentrations, and they are calculated for anion gap for their largest variability in different pathologic conditions. Anion gap is the difference between serum sodium ion and bicarbonate plus chloride. There are wide variations in the reported anion gap. Widely accepted anion gap is 8–12 mmol/L [15]. Anion gap is clinically important for assessing acidosis. Normal anion gap (hyperchloremic) acidosis and increased anion gap acidosis [27] are two important types of anion gap acidosis. Common serum cation levels are sodium 138.8 ± 4.56 mmol/L, potassium 4.05 ± 0.21 mmol/L, magnesium 0.98 ± 0.05 mmol/L [ 28] and calcium 2.2–2.7 mmol/L [ 29]. And normal serum anion levels are chloride 97.7 ± 3.42 mmol/L and acetate 0.23 ± 0.04 mmol/L [ 28]. The sum of cations and anions should be equal (Eq. (4)).
There are other ions which are not commonly measured, are unmeasured anions and cations [30]. Under normal conditions, albumin and phosphate accounts for this anion gap. There are many clinical conditions, where urate, lactate, ketone bodies, sulfate, salicylates, penicillin’s, citrate, pyruvate, and acetates are also responsible for increased anion gap [5]. So, anion gap [31] is Eq. (5)
Presence of unmeasured anion in blood is the anion gap and it represents metabolic acidosis [32]. When unmeasured anions like lactate and pyruvate donates proton then that proton is buffered by bicarbonate. And bicarbonate consumption increases the anion gap. The most common causes include lactic acidosis, diabetic ketoacidosis, uremia and acidosis due to drugs and toxins. Methanol, propylene glycol, ethylene glycol, salicylate, and some inborn error of metabolism are other causes of unmeasured anions [33]. Both lactate and β-hydroxybutyrate are increased in both Gram-positive septiceamia [34] and starvation [35]. Krebs cycle intermediate citrate, isocitrate, malate, α-ketogluterate, succinate and D-lactate are increased in different types of acidosis. Intestinal ischemia and short bowel syndrome cause increase in D-lactate [35]. Plasma proteins are mostly anionic comprising 75% of the unmeasured anion [36, 37, 38]. Treatment with Sodium thiosulfate that has no hydrogen can cause severe metabolic acidosis [39].
It usually indicates acidosis. Increase blood lactate, ketoacidosis, uremia (in advanced renal failure), drugs (salicylate and penicillin), ethylene glycol, methanol are contributor of high anion gap acidosis. But the increase anion gap can be due to laboratory error, hyperphosphatemia [30]. Massive rhabdomyelysis, hippurate, oxalate can also cause increased anion gap acidosis [31]. Diabetes, starvation and alcohol are the most common cause of ketoacidosis. In alcoholic ketoacidosis, primary keto acid is β-hydroxybutyrate. It can be missed in conventional assessment of ketonuria. High anion gap and normal lactate level are characteristics of alcoholic acidosis [40]. Starvation alone can cause high anion gap acidosis [41]. In the third trimester of pregnancy, short period of starvation can cause ketogenesis with a very high anion gap acidosis [42]. Septic shock, hypoxemia, hypovolemic shock, cyanide, mesenteric ischemia, CO poisoning, causes hypoxic type of L-lactic acidosis [43]. Non-hypoxic, L-lactic acidosis develops from seizure, thiamine deficiency, metformin, methanol, ethylene glycol, salicylate, propylene glycol, niacin, isoniazide, iron, propofol, toluene, paraldehyde, non-nucleoside reverse transcriptase inhibitor (NNRTI) drugs [12]. Recurrent 5-oxoprolinuria from inborn errors of metabolism is a rare cause if high anion gap metabolic acidosis [44]. Uremia results from not only reduced ammonia secretion but also reduced filtration of sulfate and phosphate anions, and increases the anion gap [45]. Polyclonal gammopathies are also contributor of increased anion gap [46]. Serum albumin is an important contributor to the anion gap and hypoalbuminemia is a common comorbid condition. That is why, albumin correction is crucial for the anion gap calculation [36, 37]. To explore the cause of the metabolic acidosis anion gap must be corrected for albumin as well as lactate [43]. A high anion gap can be masked by a concomitant low anion gap results from hypoalbuminemia.
In anion gap calculation, sodium is the only cation that is measured. But, hypercalcemia, hyperkalemia and hypermagnesemia can produce significant decrements in anion gap. So, clinical correlation and correction of such abnormality is important. Plasma proteins comprise two third of the unmeasured anion, and hypoalbuminemia is a common cause for the low anion gap [31, 36, 37]. The reduced anion gap is usually seen in delusional states, hypernatremia, hypoalbuminemia, hypermagnesemia, hypercalcemia, bromide intoxication, hyperviscosity associated diseases etc. [47]. Sometimes it can be due to laboratory error, paraproteinemia [48, 49], or iodide [30, 50], gastrointestinal bicarbonate loss and diarrhea [31]. It has been reported that Lithium carbonate intoxication can also produce low or absent anion gap [51]. Non-sodium containing paraprotein IgG in multiple myeloma increase the unmeasured cations and reduce the anion gap [48, 52, 53]. Hypercalcemia and hypoalbuminemia in paraproteinemia also contribute to low anion gap [52].
Measuring anion gap is a routine for evaluating acidosis, and normal anion gap is sometimes misleading. As we know, the increase in anion gap is usual in metabolic acidosis. And acidosis is due to acid retention or ingestion. Normal anion gap acidosis is due to loss of HCO3− from the body. Hyperchloremic normal anion gap acidosis is characterized by acidosis with excess chloride ions [54]. Here, the low HCO3 level is a characteristic feature. Reduced negatively charged bicarbonate is compensated by the negatively charged chloride movement into the extracellular space, and normal anion gap is maintained. The causes of gastrointestinal and renal loss of bicarbonate are diarrhea, ureteral diversions, pancreatic and biliary fistulas, toluene ingestion, acetazolamide, ifosfamide, topiramite, tenofovir, renal tubular acidosis. These are the causes of normal anion gap acidosis. Rapid infusion of 0.9% normal saline can also cause hyperchloremic metabolic acidosis [55]. If the blood anion gap is normal, but there is acidosis, then the urinary anion gap Eq. (6) is calculated [12].
The urinary anion gap is negative in diarrhea, sodium infusion and proximal renal tubular acidosis. Whereas, positive urinary anion gap is found in both type 1 and type 4 renal tubular acidosis. Renal tubular acidosis is sometimes the only presenting feature of many chronic diseases and conditions associated with polyclonal gummopathies.
Metabolic acidosis results from gain of anions and loss of cations. Potassium chloride, hydrogen chloride, sodium chloride, arginine hydrochloride, calcium chloride, ammonium chloride, lysine hydrochloride can cause hyperchloremia and increase anion gap. Hyperphosphatemia increases the anion gap. But renal tubular acidosis [33], amiloride and triamterene cause a non anion gap hyperchloraemic acidosis and hyperkalemia due to impaired bicarbonate production.
Anion gap should be measured for all types of metabolic acidosis. High anion gap metabolic acidosis is a subtype of non-respiratory acidosis. Mnemonics were used for remembering the causes of high gap metabolic acidosis such as KUSMALE (Ketoacidosis, Uraemia, Salicylate poisoning, Methanol, ParAldehyde, Lactate, Ethylene glycol) and MUD PILES (Methanol, Metformin uremia, Diabetic ketoacidosis, Paraldehydes, iron, isoniazid, Lactate, ethylene glycol, Salicylates and starvation). As paraldehyde induced acidosis is extremely rare and recently three anion gap generating organic acid has been recognized. They are Short bowel syndrome producing D-lactic acid, chronic paracetamol use induced 5-oxoproline (or pyroglutamic acid) especially in malnourished woman and high dose propylene glycol (used in lorazepum, phenobarbital) infusions generate acidosis. Also, Iron and Isoniazid can cause lactic acidosis. So, GOLD MARK is a new acronym for metabolic acidosis [Glycols (ethylene and propylene), Oxyproline, L-lactate, D-lactate, Methanol, Aspirin, Renal failure, Ketoacidosis] [56]. Metabolic acidosis also caused by renal bicarbonate loss in type 2 renal tubular acidosis, renal dysfunction in type 4 renal tubular acidosis, type 1 renal tubular acidosis and ingestion of ammonium chloride [31]. Acute rheumatism causes lactate induced acidosis also [57]. Symptomatic correction of acidosis will not eliminate the problem. If the clinical features suggest acidosis, then it should be assessed for anion gap as well. Following anion gap measurement accordingly history of drug, toxins and diseases need to be evaluated for managing the exact pathology thus acidosis will be properly treated.
At normal blood pH 7.4 plasma proteins are mostly anionic. It has been estimated that anion gap decreases by 2.5 mEq/L for every 10 gm/L drop of serum albumin [36, 37]. Several studies had observed that 2–2.5 times changes in albumin influences in anion gap changes [58]. Albumin contributes a greater part of the normal anion gap [46]. Phosphate and lactate contribute some anion gap as well [59]. Consideration of all of these contributors are important in explaining changes in anion gap. Calculation of anion gap is crucial in critically ill patients. Anion gap should be adjusted for Eq. (7) albumin, phosphate and lactate with the following equation [59].
"Open access contributes to scientific excellence and integrity. It opens up research results to wider analysis. It allows research results to be reused for new discoveries. And it enables the multi-disciplinary research that is needed to solve global 21st century problems. Open access connects science with society. It allows the public to engage with research. To go behind the headlines. And look at the scientific evidence. And it enables policy makers to draw on innovative solutions to societal challenges".
\n\nCarlos Moedas, the European Commissioner for Research Science and Innovation at the STM Annual Frankfurt Conference, October 2016.
",metaTitle:"About Open Access",metaDescription:"Open access contributes to scientific excellence and integrity. It opens up research results to wider analysis. It allows research results to be reused for new discoveries. And it enables the multi-disciplinary research that is needed to solve global 21st century problems. Open access connects science with society. It allows the public to engage with research. To go behind the headlines. And look at the scientific evidence. And it enables policy makers to draw on innovative solutions to societal challenges.\n\nCarlos Moedas, the European Commissioner for Research Science and Innovation at the STM Annual Frankfurt Conference, October 2016.",metaKeywords:null,canonicalURL:"about-open-access",contentRaw:'[{"type":"htmlEditorComponent","content":"The Open Access publishing movement started in the early 2000s when academic leaders from around the world participated in the formation of the Budapest Initiative. They developed recommendations for an Open Access publishing process, “which has worked for the past decade to provide the public with unrestricted, free access to scholarly research—much of which is publicly funded. Making the research publicly available to everyone—free of charge and without most copyright and licensing restrictions—will accelerate scientific research efforts and allow authors to reach a larger number of readers” (reference: http://www.budapestopenaccessinitiative.org)
\\n\\nIntechOpen’s co-founders, both scientists themselves, created the company while undertaking research in robotics at Vienna University. Their goal was to spread research freely “for scientists, by scientists’ to the rest of the world via the Open Access publishing model. The company soon became a signatory of the Budapest Initiative, which currently has more than 1000 supporting organizations worldwide, ranging from universities to funders.
\\n\\nAt IntechOpen today, we are still as committed to working with organizations and people who care about scientific discovery, to putting the academic needs of the scientific community first, and to providing an Open Access environment where scientists can maximize their contribution to scientific advancement. By opening up access to the world’s scientific research articles and book chapters, we aim to facilitate greater opportunity for collaboration, scientific discovery and progress. We subscribe wholeheartedly to the Open Access definition:
\\n\\n“By “open access” to [peer-reviewed research literature], we mean its free availability on the public internet, permitting any users to read, download, copy, distribute, print, search, or link to the full texts of these articles, crawl them for indexing, pass them as data to software, or use them for any other lawful purpose, without financial, legal, or technical barriers other than those inseparable from gaining access to the internet itself. The only constraint on reproduction and distribution, and the only role for copyright in this domain, should be to give authors control over the integrity of their work and the right to be properly acknowledged and cited” (reference: http://www.budapestopenaccessinitiative.org)
\\n\\nOAI-PMH
\\n\\nAs a firm believer in the wider dissemination of knowledge, IntechOpen supports the Open Access Initiative Protocol for Metadata Harvesting (OAI-PMH Version 2.0). Read more
\\n\\nLicense
\\n\\nBook chapters published in edited volumes are distributed under the Creative Commons Attribution 3.0 Unported License (CC BY 3.0). IntechOpen upholds a very flexible Copyright Policy. There is no copyright transfer to the publisher and Authors retain exclusive copyright to their work. All Monographs/Compacts are distributed under the Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0). Read more
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\\n\\nAll scientific works are Peer Reviewed prior to publishing. Read more
\\n\\nOA Publishing Fees
\\n\\nThe Open Access publishing model employed by IntechOpen eliminates subscription charges and pay-per-view fees, enabling readers to access research at no cost. In order to sustain operations and keep our publications freely accessible we levy an Open Access Publishing Fee for manuscripts, which helps us cover the costs of editorial work and the production of books. Read more
\\n\\nDigital Archiving Policy
\\n\\nIntechOpen is committed to ensuring the long-term preservation and the availability of all scholarly research we publish. We employ a variety of means to enable us to deliver on our commitments to the scientific community. Apart from preservation by the Croatian National Library (for publications prior to April 18, 2018) and the British Library (for publications after April 18, 2018), our entire catalogue is preserved in the CLOCKSS archive.
\\n"}]'},components:[{type:"htmlEditorComponent",content:'The Open Access publishing movement started in the early 2000s when academic leaders from around the world participated in the formation of the Budapest Initiative. They developed recommendations for an Open Access publishing process, “which has worked for the past decade to provide the public with unrestricted, free access to scholarly research—much of which is publicly funded. Making the research publicly available to everyone—free of charge and without most copyright and licensing restrictions—will accelerate scientific research efforts and allow authors to reach a larger number of readers” (reference: http://www.budapestopenaccessinitiative.org)
\n\nIntechOpen’s co-founders, both scientists themselves, created the company while undertaking research in robotics at Vienna University. Their goal was to spread research freely “for scientists, by scientists’ to the rest of the world via the Open Access publishing model. The company soon became a signatory of the Budapest Initiative, which currently has more than 1000 supporting organizations worldwide, ranging from universities to funders.
\n\nAt IntechOpen today, we are still as committed to working with organizations and people who care about scientific discovery, to putting the academic needs of the scientific community first, and to providing an Open Access environment where scientists can maximize their contribution to scientific advancement. By opening up access to the world’s scientific research articles and book chapters, we aim to facilitate greater opportunity for collaboration, scientific discovery and progress. We subscribe wholeheartedly to the Open Access definition:
\n\n“By “open access” to [peer-reviewed research literature], we mean its free availability on the public internet, permitting any users to read, download, copy, distribute, print, search, or link to the full texts of these articles, crawl them for indexing, pass them as data to software, or use them for any other lawful purpose, without financial, legal, or technical barriers other than those inseparable from gaining access to the internet itself. The only constraint on reproduction and distribution, and the only role for copyright in this domain, should be to give authors control over the integrity of their work and the right to be properly acknowledged and cited” (reference: http://www.budapestopenaccessinitiative.org)
\n\nOAI-PMH
\n\nAs a firm believer in the wider dissemination of knowledge, IntechOpen supports the Open Access Initiative Protocol for Metadata Harvesting (OAI-PMH Version 2.0). Read more
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\n\nBook chapters published in edited volumes are distributed under the Creative Commons Attribution 3.0 Unported License (CC BY 3.0). IntechOpen upholds a very flexible Copyright Policy. There is no copyright transfer to the publisher and Authors retain exclusive copyright to their work. All Monographs/Compacts are distributed under the Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0). Read more
\n\nPeer Review Policies
\n\nAll scientific works are Peer Reviewed prior to publishing. Read more
\n\nOA Publishing Fees
\n\nThe Open Access publishing model employed by IntechOpen eliminates subscription charges and pay-per-view fees, enabling readers to access research at no cost. In order to sustain operations and keep our publications freely accessible we levy an Open Access Publishing Fee for manuscripts, which helps us cover the costs of editorial work and the production of books. Read more
\n\nDigital Archiving Policy
\n\nIntechOpen is committed to ensuring the long-term preservation and the availability of all scholarly research we publish. We employ a variety of means to enable us to deliver on our commitments to the scientific community. Apart from preservation by the Croatian National Library (for publications prior to April 18, 2018) and the British Library (for publications after April 18, 2018), our entire catalogue is preserved in the CLOCKSS archive.
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